Cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2018-12

AUTHORS

Seitaro Nomura, Masahiro Satoh, Takanori Fujita, Tomoaki Higo, Tomokazu Sumida, Toshiyuki Ko, Toshihiro Yamaguchi, Takashige Tobita, Atsuhiko T. Naito, Masamichi Ito, Kanna Fujita, Mutsuo Harada, Haruhiro Toko, Yoshio Kobayashi, Kaoru Ito, Eiki Takimoto, Hiroshi Akazawa, Hiroyuki Morita, Hiroyuki Aburatani, Issei Komuro

ABSTRACT

Pressure overload induces a transition from cardiac hypertrophy to heart failure, but its underlying mechanisms remain elusive. Here we reconstruct a trajectory of cardiomyocyte remodeling and clarify distinct cardiomyocyte gene programs encoding morphological and functional signatures in cardiac hypertrophy and failure, by integrating single-cardiomyocyte transcriptome with cell morphology, epigenomic state and heart function. During early hypertrophy, cardiomyocytes activate mitochondrial translation/metabolism genes, whose expression is correlated with cell size and linked to ERK1/2 and NRF1/2 transcriptional networks. Persistent overload leads to a bifurcation into adaptive and failing cardiomyocytes, and p53 signaling is specifically activated in late hypertrophy. Cardiomyocyte-specific p53 deletion shows that cardiomyocyte remodeling is initiated by p53-independent mitochondrial activation and morphological hypertrophy, followed by p53-dependent mitochondrial inhibition, morphological elongation, and heart failure gene program activation. Human single-cardiomyocyte analysis validates the conservation of the pathogenic transcriptional signatures. Collectively, cardiomyocyte identity is encoded in transcriptional programs that orchestrate morphological and functional phenotypes. More... »

PAGES

4435

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41467-018-06639-7

    DOI

    http://dx.doi.org/10.1038/s41467-018-06639-7

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1107733458

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/30375404


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